Topic
Acyl-CoA
About: Acyl-CoA is a research topic. Over the lifetime, 527 publications have been published within this topic receiving 25134 citations. The topic is also known as: Acyl Coenzyme A.
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TL;DR: Trans-2-enoyl-CoA hydratase can perform a reversible hydration of α, β-unsaturated fatty acid chain elongation and is reported to have been reported from rat liver and from rat mitochondria.
Abstract: It is well known that fatty acid chain elongation involves four steps : (a) condensation of a primer with malonyl-CoA to form the β-keto acyl CoA; (b) reduction of the resulting β -keto acyl CoA to a secondary alcohol, β-hydroxyl acyl CoA; (c) dehydration of the alcohol to form trans-2-enoyl CoA; and (d) reduction of the trans-2-enoyl CoA to give an acid 2 carbon atoms longer than the primer. 1–2The enzyme involved in step (c) is trans-2-enoyl-CoA hydratase, It can perform a reversible hydration of α, β-unsaturated fatty acid chain elongation. 3A partial purification of this enzyme has been reported by Bernert and Sprecher. 4The purification of enoyl-CoA hydratase from mycobacterium smegmatis 5and from rat mitochondria have also been reported; 6however, the purification of enoyl-hydratase from rat liver has not been reported.
3 citations
TL;DR: The rate of beta-oxidation of C-6-C-10-fatty acids was several times higher in homogenates from clofibrate-treated rats than in control rats, both in the presence and absence of 2.0 mmol l-1 cyanide.
Abstract: The beta-oxidation of C-6-C-10-fatty acids/acyl CoA/acylcarnitines in whole rat liver homogenates was determined by specific and simultaneous measurements of the C-6-C-10-fatty acids, i.e. hexanoic, octanoic and decanoic acids, in hydrolysed homogenates in relation to time in assays incubated with the above-mentioned substrates. Measurements were performed by a combined gas chromatographic mass spectrometric technique, i.e. selected ion monitoring. The rate of beta-oxidation of the C-6-C-10-fatty acids/acyl CoA/acylcarnitines were registered as the consumption rate of the added substrate. The conversion to the C-2-shortened beta-oxidation products was illustrated simultaneously. The rate of beta-oxidation of C-6-C-10-fatty acids was several times higher in homogenates from clofibrate-treated rats than in control rats, both in the presence and absence of 2.0 mmol l-1 cyanide. Cyanide caused a minor but significant decrease in the beta-oxidation rate in both control and clofibrate-treated rats. No differences were found between the beta-oxidation of decanoic acid and decanoyl CoA in homogenates from clofibrate-treated rats, whereas the degree of beta-oxidation of DL-decanoylcarnitine was halved compared with decanoic acid and decanoyl CoA.
3 citations
TL;DR: There were no significant differences between control and patient membranes, suggesting that abnormalities in these 3 putative candidate enzymes are not responsible for the disease.
Abstract: In order to study the biochemical mechanisms responsible for the membrane fatty acid deficiency in juvenile neuronal ceroid-lipofuscinosis, we have analyzed the reacylation pathway in isolated erythrocyte membranes in 5 patients. We studied membrane carnitine palmitoyl transferase, and developed a combined assay to study acyl-CoA synthetase and lysophospholipid acyl-CoA acyltransferase activities. There were no significant differences between control and patient membranes, suggesting that abnormalities in these 3 putative candidate enzymes are not responsible for the disease.
3 citations
TL;DR: Inhibition of both enzymes was observed when clofibrate, or the tetrahydronapthyl analog of this drug were added in vitro, and the inhibitory effects were most pronounced on the fatty acyl CoA:cholesterol acyltransferase.
2 citations
TL;DR: In this article , the authors present an in vitro acylation assay with purified hedgehog acyltransferase (Hhat) that directly monitors attachment of a fluorescently tagged fatty acyl chain to Shh.
2 citations